How to Get Published in Science A GUIDE

How to Get Published in Science A GUIDE TO SCIENTIFIC WRITING

The Science Family of Journals Mission: Seeking to publish papers that are most influential in their fields or across fields and that will significantly advance scientific understanding. Selected papers should present novel and broadly important data, syntheses or concepts. They should merit the recognition by the scientific community and general public.

2015 -2016年Science发文情况 时间 期刊 国家 USA 2015 -2016 Science 发文量 排名 2190 1 ENGLAND 520 2 GERMANY 437 3 FRANCE 261 4 PEOPLE R CHINA 232 5 CANADA 210 6 SWTZERLAND 186 7 JAPAN 170 8 NETHERLANDS 165 9 AUSTRALIA 156 10

2015 -2016年Science Signaling发文情况 时间 期刊 国家 USA 2015 -2016 Science Signaling 发文量 排名 252 1 GERMANY 53 2 ENGLAND 37 3 FRANCE 34 4 PEOPLE R CHINA 27 5 CANADA 22 6 JAPAN 19 7 SWEDEN 15 8 AUSTRALIA 14 9 SPAIN 12 10

2015 -2016年Science Translational Medicine发文情况 时间 期刊 国家 USA 2015 -2016 Science Translational Medicine 发文量 排名 470 1 ENGLAND 90 2 GERMANY 69 3 FRANCE 45 4 SWTZERLAND 38 5 CANADA 38 6 ITALY 37 7 PEOPLE R CHINA 33 8 NETHERLANDS 33 9 AUSTRALIA 32 10

Submitting to the Science Family of Journals

How to Publish in the Science Journals is NOT a secret 考虑以下几个因素_audience § Know your audience 你所研究领域的科学家 你所研究领域之外的科学家 评审 编辑 出版社及公众

Total Submissions and Acceptance Rate 2016 投稿数量 > 11500 > 700 > 2600 接收率 6% 19% 7% 2000 16%

YOU CANT GO WRONG § IF YOUR PAPER IS NOT SUITABLE FOR ONE SCIENCE FAMILY JOURNAL, WE WILL HELP YOU TRANSFER TO A MORE SUITABLE SCIENCE JOURNAL

Science数据库中OA刊与非OA刊的区别 Gold Open Access § 作者支付很小一部分费用 § 作者付费 § 须订阅 § 对用户不收费，一旦发表即可阅读 § 对单独用户可提供单篇订购方式 Science Advances Science Signaling Science Translational Medicine Science Immunology Science Robotics

稿件评审的一般流程（Review process) Manuscript submission Referees consulted Accepted (~ ? %) Rejected (~ ? %) Editorial rejection (~ ? %) Decision letter resubmission?

Practical tips to getting published A GUIDE TO SCIENTIFIC WRITING

5 Golden Rules § Know your audience § Write clearly § Write concisely § Write accurately § Follow instructions

Write clearly Avoid imprecise words § Regulates § Alters § Influence Avoid words with multiple meanings § Levels § Elevates § Significant Avoid lab jargon

Rewrite and edit for clarity Make sure that every word in every sentence says what you really mean!

举例：原始文章 Abstract 109 words Pathogenic mutations in leucine-rich repeat kinase 2 (LRRK 2) are the most common genetic cause of late onset Parkinson’s disease (PD). There was mounting evidence that the intrinsic kinase activity of LRRK 2 is required for LRRK 2 -mediated PD pathogenesis. However, recent studies suggested that LRRK 2 kinase activity is dispensable for neuron survival and its protective activity against the neurotoxin. It was hypothesized that LRRK 2 kinase domain might have a scaffolding role independent of its intrinsic kinase activity in the assembly of signaling complexes. In this regard, the intrinsic kinase activity of LRRK 2 appears to be a Trojan horse for PD and modulation of its kinase activity could be potentially therapeutically beneficial.

Edited

Final Abstract 83 words Pathogenic mutations in leucine-rich repeat kinase 2 (LRRK 2) are common genetic causes of late onset Parkinson’s disease (PD). Initial studies indicated that the intrinsic kinase activity of LRRK 2 is associated with LRRK 2 -mediated PD pathogenesis. However, the kinase activity of LRRK 2 may be dispensable for neuron survival and may not be required for its protective activity against neurotoxicity. Thus, the intrinsic kinase activity of LRRK 2 appears to be a Trojan horse for PD and inhibition of its kinase activity could be potentially therapeutically beneficial.

Research Article Abstract: Before (224 words) Cells derived from ataxia telangiectasia (A-T) patients exhibit defective cell cycle checkpoints following ionizing radiation (IR), profound radiosensitivity and high levels of chromosome aberrations. We have shown that transient ATM kinase inhibition from +15 to +75 min following IR is sufficient to radiosensitize cells and accumulate persistent chromosome aberrations. We show here that DNA-PK kinase inhibition from +15 to + 75 min is also sufficient to radiosensitize cells and accumulate persistent chromosome aberrations. The ATM kinase-dependent mechanisms that ensure cell survival and suppress chromosome aberrations during this interval are independent of DNA-PK kinase activity. Neither the activation nor the recovery of the IR-induced G 2/M cell cycle checkpoint are affected by ATM kinase inhibition from +15 to +75 min, indicating that 15 min of ATM kinase signaling is sufficient to induce this cell cycle checkpoint. Surprisingly, ATM kinase inhibition from +15 to +75 min abrogates IR-induced sister chromatid exchange (SCE), a phenotype attributed to the repair of damaged replication forks. Further, ATM kinase inhibition using either KU 55933 or KU 60019 is sufficient to disrupt camptothecin-induced SCE. Since DNA damage-induced SCE is maintained A-T cells that express no ATM protein, and the ATM kinase inhibitors have no effect on DNA damage-induced SCE in A-T cells, these data reveal that the consequences of acute ATM kinase inhibition and adaptation to ATM protein disruption are distinct in S-phase cells.

Problems Cells derived from ataxia telangiectasia (A-T) patients exhibit defective cell cycle checkpoints following ionizing radiation (IR), profound radiosensitivity and high levels of chromosome aberrations. § What is radiosensitivity? § What is the relationship of radiosensitivity to chromosome aberrations? We have shown that transient ATM kinase inhibition from +15 to +75 min following IR is sufficient to radiosensitize cells and accumulate persistent chromosome aberrations. § ATM kinase = The kinase that phosphorylates ATM? We show here that DNA-PK kinase inhibition from +15 to + 75 min is also sufficient to radiosensitize cells and accumulate persistent chromosome aberrations. § What are ATM and DNA-PK? § DNA-PK kinase = The kinase that phosphorylates DNA-PK? NO The ATM kinase-dependent mechanisms that ensure cell survival and suppress chromosome aberrations during this interval are independent of DNA-PK kinase activity. § ATM kinase-dependent = Mechanisms that rely on phosphorylation of ATM? NO § How does cell survival relate to radiosensitivity?

More problems Neither the activation nor the recovery of the IR-induced § What is the IR-induced G 2/M checkpoint? G 2/M cell cycle checkpoint are affected by ATM kinase inhibition from +15 to +75 min, indicating that 15 min of ATM kinase signaling is sufficient to induce this cell cycle checkpoint. Surprisingly, ATM kinase inhibition from +15 to +75 min § abrogates IR-induced sister chromatid exchange (SCE), a phenotype attributed to the repair of damaged replication forks. Further, ATM kinase inhibition using either KU 55933 or KU 60019 is sufficient to disrupt camptothecin-induced SCE. Why is this surprising? What do damaged replication forks have to do with IR-induced damage? § Too much experimental detail. § What is camptothecin?

And more problems Since DNA damage-induced SCE is maintained A-T cells that express no ATM protein, and the ATM kinase inhibitors have no effect on DNA damage-induced SCE in AT cells, these data reveal that the consequences of acute ATM kinase inhibition and adaptation to ATM protein disruption are distinct in S-phase cells. § Since should be because. § Genes are expressed, not proteins. § The information about S-phase is out of context.

Did your eyes glaze over? § Lack of context § Too much methodological detail § Imprecise language § Too many undefined terms

Clean edited version with editorial queries (182 words)

Practice § Although most PD cases are sporadic, at least seven genes have been reported to be implicated in the pathogenesis of familial PD (1). (hint: too many words) § In vitro studies indicated that several pathogenic mutations in LRRK 2 caused an increase in the kinase activity, such as mutations R 1441 C in ROC GTPase domain and G 2019 S in kinase domain (4 -6). (hint: multiple problems, including a misplaced clause) § While the physiological function of LRRK 2 remains largely unknown, recent studies indicated a dispensable role of the intrinsic kinase activity of LRRK 2 in neuron survival and its protective activity against neurotoxin (10 -12). (hint: multiple problems, especially temporal words) § The current paper reports for the first time a sex reversal in transsexual people in the interstitial nucleus of the anterior hypothalamus (INAH) 3, a sexually dimorphic hypothalamic nucleus that was previously shown to be related to sexual orientation (citation 1, citation 2).

Categories of manuscripts § 《科学》周刊的栏目（论文分类） § 评论 Reviews § 研究文章 Research Articles § 报告 Reports § 技术评论 Technical Comments § 信件 Letters § 政策论坛 Policy Forum § 教育论坛 Education Forum § 书评 Books § 研究述评 Perspectives